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STEP 1

1. Lump : benjolan. A piece of solid substance usually with no particular shape


2. Palpitations : denyutan. A condition in which your heart beat too quickly or not
regularly
3. Stool frequency : a seat without any support for the back or arms (stool)
4. Tremor : unintentional trembling or shaking movement in one or more parts of your
body
STEP 2
1. Cause of weight loss
2. Clinical Manifestation
3. What cause a trembling hands
4. What is the patogenesis
5. Why she cant stand the heat ?
6. How to diagnose for hyperthyroid ?
7. What is the differential diagnose from the scenario ?
8. What are the treatment ?
9. Etiology ?
10. Diagnosis
11. What is biosynthesis of T3 and T4 ?
12. Definition of hyperthyroidism
13. Why the patient have that clinical manifestation ? explain
14. Krisis tiroid ?
15. Explain the hypothyroid
STEP 3
1. What is biosynthesis of T3 and T4 ?
Phase trapping iodide : bassal cell membranes ability to pump specific
thyroid iodide actively to the inside of the cell ( iodide transport from the
blood into the cells and follicular thyroid glands).
Oxidation stage : change of iodide ion into the oxide from of iodine, iodine
either early (nascent iodine) which then is able to bind with the amino acid
thyrosine.
This process is enhanced by and accompany peroxidase and hydrogen peroxidase
Phase organification thyroglobulin the binding of iodine with the
thyroglobuline molecule iodinate thyrosin process sequency :
Thyrosine diioidnized be monoidothyrosine, then became diiodithyrosine
Occurs chopping of the remaining diiodothyrosine the result of which from the
thyroxine molecule
Thyroglobulin storage stage : thyroid hormones are stored in the follicle in
sufficient quantities to supply the body with the bodies normal requirements for
thyroid hormone for 2-3 months
Thyroxine and triiodothyronine release phase of the thyroid gland : thyroglobulin
wasnt released in the blood, thyroxine and triiodothyronine thyroglobuline be
broken from the free hormone is then release into the blood
2. Cause of weight loss
The occurance because of levels of hypermetabolic inside the body where the tyroid
hormone stimulates lipolysis.
3. Why she cant stand the heat ?

Because at the time of hormon thyroid increases activate 1 enzyme (Na+ K+ ATPase) which cause increase Na+ transport forth and K+ through the cell membran.
Because this process requires energy and increase the amount of heat that is formed in
the body which is one cause of the increase body metabolism because at HT
increasedcause increase mitocondrial size and activity leading to increase
metabolism
4. What cause a trembling hands
Increased thyroid hormone increase sensitivity nerve synaps in medulla that
regulate muscle tone.
5. How to diagnose ?
Physical examination revealed
a. High systole blood pressure
b. Hyperactive reflects
c. Increase heart rate
d. Tremor
In the other hand, blood test also done to measure levels of thyroid hormons ex : TSH,
T3 and T4. And it can be this disease may also effect the result of the following test,
ex : glucotest, cholesterol test, radioactive iodine uptake
Test :
a. Serum TSH level where measure by radioimmunometric
b. Uptake of iodine radioisotop to measure the ability of gland
c. Thyroid scan
6. What is the differential diagnose from the scenario ?
a. Euthyroid hyperthyroxinemia Goiter
b. Grave disease
c. Plummer-Vinson syndrome
d. Struma ovarii
e. Tirotoksikosis
7. Diagnosis
Hyperthyroidism
8. Definition of hyperthyroidism
Hyperthyroidism is a condition in which the thyroid gland makes too much thyroid
hormon, the condition is often reffered as an over active thyroid
Hyperthyroidism is a case hypermetabolic that cause increase some endocrine in the
thyroid gland, ex : tiroksin, and triiodotiroksin (T3 and T4)
9. Etiology ?
Graves disease
Tirotoksikosis
Ophtalmophaty infiltrative
Dermophaty Infiltrative
Toxic Multi Nodular Goiter
Solitary toxic adenoma

Hyperthyroidism caused by disfunction of thyroid gland . increased TSH thyroid


gland malfunction to be accompanied by decrease TSH and TRF as a negative
feedback HT on the release of a both
10. What is the pathogenesys
As in autoimmune hyperthyroidism a combination of environmental and genetic
factor including polymorfism in HLA-DR CTLA-4 CD-25 PTTN-22 and TSHR
contribute to briefs disease susceptibility the concordance for Graves disease in
monozygote twins is 20-40% compared to <5% in dizygote twins indirect evidence
suggest stress is an important environmental factor presumably operating throughn
neuroendocrine effects on the immune system.
11. Clinical Manifestation
a. Sudden weight loss
b. Tachycardia/rapid heart beat
c. Increase appetite
d. Tremor
e. Sweating
f. Difficulty sleeping
g. Skin thinning
h. Increase sensitivity to heat
i. Lump in the neck area
12. What are the treatment ?
Hyperthyroidsim is usualy treat with one/more of the following :
a. Anti-thyroid medication (prevent thyroid hormon synthesis : inhibiton of
peroxidase, thereby inhibiting organification)
Propiltiourasil
Metimazol
Carbimazole

b.
c.
d.
e.
f.

Indication : hyperthyroidism
Contraindication : tracheal damage, lactating mothers, hypersensitivity
Radioactive iodine (emission of beta rays will damage the thyroid gland
tissues that hormon production is reduce)
If the patient is >35 years old
Surgery to remove the thyroid
Inhibition anion group ( iodide uptak inhibition mechanism competitively
inhibit iodide transport)
Iodide (organification inhibit iodide and release of T3 and T4 hormon)
Beta blockers, this drugs not for hyperthyroid but for the symptoms
(tachycardia) and help prevent palpitation.

If the thyroid must be removed with surgery or radioactive we must take thyroid hormon
replacement pil for the rest of our live and in the other hand beta blockers such as propanolol
are used to treatment some of the symptomps including rapid heart rate and ancient until the
hyperthyroidism can be controlled.
13. Why the patient have that clinical manifestation ? explain
Palpitation : T3 adn T4 increase metabolism up accelerate oxygen using increase
releasing the amount of final product from tissue metabolism catabolism in long

time vasodilatation increase blood stream power of cardiac muscle is forced


(ditekan) increase heat rate frequency and kerja jantung meningkat >60%
14. Uncommon medical emergency caused by an exacerbation of hyperthyroidsim
characterized of one or more organ system in people with untreated and or poorly
treated hyperthyroidism. Hyperthyroid disease crisis usually occur in patient already
known to have hyperthyroidism but may be the first presentation of hyperthyroidism
early recognition and agressive treatment are essential.hyperthyroidism can occur in
patient w/ toxic adenoma or multinodular toxic goiter but its more often see in grave
disease. Hyperthyroidism crisis classically occurs in patient w/ underlying grave
disease or toxic multi nodular goiter often there is sudden onset of sever
hyperthyroidism with first hyperpyrexia over 41 celcius, dehidration, heart rate
greater 140/minutes, naussea, jundice, abdominal pain, confussion, seizeres(kejang),
comma

Uptake tsh >>> tsi <<<

Clinical manifestation

Laboratory checking

Treatment

STEP 7
1. What is biosynthesis of T3 and T4 ?
Phase trapping iodide : bassal cell membranes ability to pump specific
thyroid iodide actively to the inside of the cell ( iodide transport from the
blood into the cells and follicular thyroid glands).
Oxidation stage : change of iodide ion into the oxide from of iodine, iodine
either early (nascent iodine) which then is able to bind with the amino acid
thyrosine.
This process is enhanced by and accompany peroxidase and hydrogen peroxidase
Phase organification thyroglobulin the binding of iodine with the
thyroglobuline molecule iodinate thyrosin process sequency :
Thyrosine diioidnized be monoidothyrosine, then became diiodithyrosine
Occurs chopping of the remaining diiodothyrosine the result of which from the
thyroxine molecule
Thyroglobulin storage stage : thyroid hormones are stored in the follicle in
sufficient quantities to supply the body with the bodies normal requirements for
thyroid hormone for 2-3 months
Thyroxine and triiodothyronine release phase of the thyroid gland : thyroglobulin
wasnt released in the blood, thyroxine and triiodothyronine thyroglobuline be
broken from the free hormone is then release into the blood
2. Cause of weight loss

Increased sympathetic activity and hypermetabolism causes weight loss


despite increased appetite.
Robbins n 'Kumar. PATHOLOGY. Vol 2. Edition 7. EGC
Mengapa bb turun walau nafsu makan bertambah?
Peningkatan aktivitas simpatis dan hipermetabolisme menyebabkan penurunan BB
walaupun nafsu meningkat.
Robbins n Kumar. PATOLOGI. Vol 2. Edisi 7. EGC
3. Why she cant stand the heat ?

Because BMR ride that ride thermogenesis. So the body can not stand the
heat.
Because of the patient's skin tends to soft thyrotoxicosis, warm, and
redness, patients often do not stand the heat.
Robbins n Kumar. PATOLOGI. Vol 2. Edisi 7. EGC

Mengapa tdk tahan panas ?


Karena BMR naik sehingga thermogenesis naik. Jadi tubuh tidak tahan panas.
Karena pada kulit pasien tirotoksikosis cenderung lunak, hangat, dan kemerahan,
pasien sering tidak tahan panas.
Robbins n Kumar. PATOLOGI. Vol 2. Edisi 7. EGC
4. What cause a trembling hands

Increased thyroid hormone can also increase the strong muscle


contractions cause smooth muscle tremor, which is a typical
symptom of hyperthyroidism
Due to increased sensitivity of the nerve synapse in the medulla
that regulate muscle tone.
Buku Ajar Fisiologi Guyton

Mengapa tangan gemetar?


Peningkatan hormon tiroid juga dapat meningkatkan
kontraksi otot yang kuat menimbulkan tremor halus
pada otot, yang merupakan gejala khas hipertiroidisme

Disebabkan bertambahnya kepekaan sinaps syaraf di daerah


medulla yg mengatur tonus otot.
Buku Ajar Fisiologi Guyton
5. How to diagnose ?
Physical examination revealed
e. High systole blood pressure
f. Hyperactive reflects
g. Increase heart rate
h. Tremor
In the other hand, blood test also done to measure levels of thyroid hormons ex : TSH,
T3 and T4. And it can be this disease may also effect the result of the following test,
ex : glucotest, cholesterol test, radioactive iodine uptake
Test :
d. Serum TSH level where measure by radioimmunometric
e. Uptake of iodine radioisotop to measure the ability of gland
f. Thyroid scan
6. What is the differential diagnose from the scenario ?
f. Euthyroid hyperthyroxinemia Goiter
g. Grave disease
h. Plummer-Vinson syndrome
i. Struma ovarii
j. Tirotoksikosis
7. Diagnosis
Hyperthyroidism
8. Definition of hyperthyroidism
a. Hyperthyroidism refers to conditions caused by excessive thyroid hormone produced
by thyroid gland
b. Most common causes of hyperthyroidism are Graves disease, toxic multinodular
goiter, toxic uninodular goiter, and thyroiditis

c.

Less common causes of hyperthyroidism are thyroid-stimulating hormone (TSH)producing tumors, pituitary resistance to thyroid hormone, trophoblastic disease, and
iodine ingestion
d. Signs and symptoms generally result from stimulation of adrenergic nervous system
e. Overt hyperthyroidism is defined as low serum TSH with elevated peripheral thyroid
hormone values (free T3 and/or free T4), while subclinical hyperthyroidism is defined
as low serum TSH with normal peripheral thyroid hormone values

https://www.clinicalkey.com/topics/endocrinology/hyperthyroidism.html
Hyperthyroidism occurs due to an overactive thyroid gland.
In newborns, the cause of hyperthyroidism is the most common neonatal Graves
disease. This disease can be fatal and can occur in infants whose mothers suffer or
have ever suffered from Graves' disease.
Graves' disease is an autoimmune disease in which the body produces antibodies that
stimulate the thyroid gland.
In pregnant women, these antibodies can be up to stimulate the fetus and the fetal
thyroid gland.
Graves' disease in the mother can lead to stillbirth, miscarriage or premature birth.
In newborns, the symptoms of an overactive thyroid gland can occur within a few
days after birth:
- Do not gain weight
- Rapid heartbeat
- High blood pressure
- Fussy or restless
- vomiting
- Diarrhea.
Mumps can suppress airway and interfere with breathing.
High levels of thyroid hormone can cause rapid heart rate which in turn can lead to
heart failure.
As with adults, the newborn, the eyes also stand out.
If the treatment is done, the recovery will happen in a few weeks, but the baby still
has a risk of recurrence for 6 months to 1 year.
Thyroid stimulating antibody levels remained high can also cause premature closure
of the fontanel, mental retardation, hyperactivity in childhood and slow growth.
Hyperthyroidism treated with propylthiouracil medicine, which serves to inhibit the
formation of thyroid hormones.
May also need treatment for heart failure.
If the levels of TSH (thyroid-stimulating hormone) is very high, it may be necessary
to replace blood transfusions (number of infant blood removed and replaced with
blood from a donor).
WWW.MEDICASTORE.COM
Hipertiroidisme
Hipertiroidisme terjadi karena kelenjar tiroid yang terlalu aktif.
Pada bayi baru lahir, penyebab dari hipertiroidisme yang paling sering ditemukan

adalah penyakit Graves neonatorum. Penyakit ini bisa berakibat fatal dan bisa terjadi
pada bayi yang ibunya menderita atau pernah menderita penyakit Graves.
Penyakit Graves adalah suatu penyakit autoimun dimana tubuh menghasilkan
antibodi yang merangsang kelenjar tiroid.
Pada wanita hamil, antibodi ini bisa sampai ke janin dan merangsang kelenjar tiroid
janin.
Penyakit Graves pada ibu bisa menyebabkan lahir mati, keguguran atau kelahiran
prematur.
Pada bayi baru lahir, gejala kelenjar tiroid yang terlalu aktif bisa timbul dalam waktu
beberapa hari setelah lahir:
- berat badan tidak bertambah
- denyut jantung yang cepat
- tekanan darah tinggi
- rewel atau gelisah
- muntah
- diare.
Gondok bisa menekan saluran udara dan mengganggu proses bernafas.
Kadar hormon tiroid yang tinggi bisa menyebabkan denyut jantung menjadi cepat
yang selanjutnya dapat menyebabkan gagal jantung.
Seperti halnya pada dewasa, pada bayi baru lahir, mata juga menonjol.
Jika dilakukan pengobatan, pemulihan akan terjadi dalam beberapa minggu, tetapi
bayi tetap memiliki resiko kekambuhan selama 6 bulan sampai 1 tahun.
Kadar antibodi perangsang tiroid yang tetap tinggi juga dapat menyebabkan
penutupan dini ubun-ubun, keterbelakangan mental, hiperaktivitas pada masa kanakkanak dan pertumbuhan yang lambat.
Hipertiroidisme diobati dengan obat propilthiouracyl, yang berfungsi menghambat
pembentukan hormon tiroid.
Mungkin juga perlu dilakukan pengobatan terhadap gagal jantung.
Jika kadar TSH (thyroid-stimulating hormone) sangat tinggi, mungkin perlu dilakukan
transfusi darah ganti (sejumlah darah bayi dibuang dan diganti dengan darah dari
donor).
WWW.MEDICASTORE.COM
9. Etiology ?
a. Toxic diffuse goiter or Graves disease (most common cause): an autoimmune
disease in which thyroid gland is being stimulated by thyrotropin receptor antibodies,
also known as thyroid-stimulating immunoglobulin
b. Toxic multinodular goiter: multiple areas in thyroid gland overproduce thyroid
hormone independently of TSH
c. Toxic uninodular goiter (adenoma): solitary nodule in thyroid gland overproducing
thyroid hormone independently of TSH
d. Subacute thyroiditis: usually idiopathic but sometimes can be result of virally mediated
inflammation and destruction of thyroid gland. Consequently, stored thyroid hormones
are released into circulation, causing transient thyrotoxic state and thyroid pain
e. Postpartum or sporadic thyroiditis: painless autoimmune inflammation of thyroid
gland, in which stored thyroid hormones are released into circulation, causing a
transient thyrotoxic state
f. Amiodarone-induced (types I and II): Type I is iodine-induced, while Type II is type of
thyroiditis

g. Iatrogenic or factitious thyrotoxicosis: due to intentional or inadvertent ingestion of


exogenous thyroid hormone

https://www.clinicalkey.com/topics/endocrinology/hyperthyroidism.html
10. What is the pathogenesys
The pathogenesis of hyperthyroidism
The major question to be solved in the pathogenesis of hyperthyroidism is the
mechanism
responsible for oversecretion by the thyroid
gland.
Various views have been held in the past depending on successive advances in
physiology
and biochemistry. Charcot (1856) regarded the
condition as a neurosis until Moebius pointed
out the associated goitre. The demonstration that
iodine was a component of the thyroid gland
by Baumann in 1895 led eventually to the postulate that the disorder was essentially
one of
iodine metabolism. The demonstration by Cannon of the physiological effects of
adrenaline
led to the postulate of a mechanism via the sympathetic nervous system. The
recognition of
pituitary thyroid control and preparation of
potent pituitary extracts by Evans, Smith and
Smith and others in the early 1920s led to the
claim of experimental production of exophthalmos
and hyperthyroidism in the rat by pituitary extracts (Marine & Rosen, 1934). These
findings
led to the postulate of hyperpituitarism as the
mechanism of the disorder (Marine, 1935).
A characteristic feature, recognized after 1950,
is that the hypersecreting gland is not suppressed
by the administration of thyroxine or triiodothyronine, even in very large doses, in
contrast to
the normal gland (Werner, 1955). While this property is not always associated with
elevated
levels of circulating thyroid hormones it usually
is. Where it is not the gland is hypersecreting
from a small pool of hormone due to previous
surgery, or thyroiditis due to various causes
(Liddle, Heyssel & McKenzie, 1965). This property suggested to Werner (1955) that
the thyroid gland itself was at fault and not the pituitary trophic hormone secretion.
The high effectiveness of therapy for thyrotoxicosis based on partial ablation of the
thyroid
gland contrasts strikingly with the tendency to
recurrence of hyperadrenalism following partial
ablation of hyperplastic adrenal glands; this observation was in keeping with the
suggestion that
the disorder resided within the thyroid itself.

Plummer had originally suggested that exophalmic goitre patients were suffering from
'dysthyroidism' or an abnormal thyroid secretion
(Means, 1937). This and other similar postulates
raises the question of the nature of thyroid
secretion in thyrotoxicosis.
http://pmj.bmj.com/content/44/511/363.full.pdf
11. Clinical Manifestation
Common complaints include fatigue, heat intolerance, sweating, weight loss
despite good
appetite, shakiness, inappropriate anxiety, palpitations of the heart, shortness of
breath, tetchiness
and agitation, poor sleep, thirst, nausea and increased frequency of defecation. The
elderly may
complain predominantly of heart problems with a fast or irregular heart beat,
breathlessness and
ankle swelling, whereas children tend to hyperactivity, with a short attention span.
Signs include
shaky and hot hands, fast or irregular heart beat, inability to sit still, flushing of
the face and upper
trunk, fast tendon reflexes, an enlarged thyroid gland and prominent or bulging
eyes. Nowadays
patients often are diagnosed at an early stage of disease, owing to increased
awareness and
improved biochemical testing. Therefore some patients have relatively few of the
classical signs
or symptoms. In addition, none of the symptoms or signs just listed is sufficiently
sensitive or
specific for the diagnosis of hyperthyroidism, even when combined together.
Thus, it may take
three to six months to diagnose hyperthyroidism, during this time the person can
feel very unwell.
It is not uncommon for people to worry that they have cancer, because of the
associated weight
loss.
http://www.british-thyroid-association.org/info-forpatients/Docs/bta_patient_hyperthyroidism.pdf
12. What are the treatment ?
Betablockers
Betablockers are a group of drugs that tend to improve some of the symptoms and
manifestations
of hyperthyroidism. In particular, they can improve palpitations, slow the heart down
and improve
tremor. They have no effect on curing the thyroid overactivity, but do make many
people feel
better. Betablockers should not be taken if the patient has asthma or a wheezy chest.
Antithyroid drugs
Carbimazole (Neomercazole) and propylthiouracil are antithyroid drugs that are
effective in

reducing the production of thyroid hormones in the majority of people with


hyperthyroidism. In
people with Graves disease, treatment with one of these drugs for between 6 months
and 2 years
results in a long-term remission in around half of patients, once the drug is stopped.
Both drugs have the common side effects of rash and joint pains, and more rarely (less
than 1 in
500 cases) a serious reduction in the circulating white blood cells (agranulocytosis)
may occur
during treatment. The dosage of these antithyroid drugs can either be adjusted every 6
to 8 weeks
according to thyroid hormone levels in the blood, to keep the persons thyroid
hormone levels in
the normal range (titrated dose regimen) or kept at a fixed, higher dose and
levothyroxine
replacement added to maintain normal thyroid hormone levels (block and replace
regimen). In
nodular hyperthyroidism (solitary toxic nodule or toxic multinodular goitre),
antithyroid drugs do not
result in cure, just a temporary reduction in thyroid hormone levels. A more
permanent solution is
often sought, called a definitive treatment.
Radioiodine
Radioiodine is a radioactive isotope of iodine (
131I) that is taken up and concentrated selectively by
the thyroid gland. In most people, this small dose of radioactivity is sufficient to
gradually destroy
the thyroid tissue, over 6 weeks to 6 months following a single dose. Patients with
Graves disease
have a high rate of permanent thyroid underactivity following radioiodine (about
80%), whereas
patients with nodular thyroid overactivity tend to preserve their thyroid function
better, with only
around half eventually becoming underactive. Patients are monitored for underactivity
following
the dose and promptly treated with thyroxine, should this develop. The common
outcome of
thyroid underactivity is an accepted consequence of radioiodine therapy because
hyperthyroidism
is a serious condition whereas replacement treatment with levothyroxine is simple and
has no side
effects at the correct dose.
Radioiodine is a safe treatment for thyroid overactivity, with no overall excess of
cancers in many
hundreds of thousands of patient years of follow up (JAMA 1998; 280: 347-355;
Lancet 1999; 353:
2111-5). Patients with ophthalmopathy require careful evaluation, as radioiodine may
worsenthyroid eye disease: this can be prevented by a short course of steroid tablets.
There is no

damage to fertility or to hair growth, but women are advised not to become pregnant
for 6 months
following a dose, as the babys thyroid could be damaged. Men should avoid fathering
a child
within 4 months of treatment. Following a standard dose of radioiodine, other
precautions are
necessary to minimise radiation exposure of others but these restrictions are usually
easily
accommodated by the patient. Radioiodine may trigger airport security alarms up to
eight weeks
following a dose and patients should carry a letter about the treatment if they travel in
this period.
Radioiodine is the most cost effective and certain treatment for thyroid overactivity
and about
10,000 doses annually are given in the UK.
Thyroid surgery
Surgery to remove most or all of the thyroid gland (subtotal or total thyroidectomy) is
another way
of definitively treating thyroid overactivity. This is a straightforward operation when
carried out by
an experienced thyroid surgeon, with a low risk of complications. Hypothyroidism is
a recognised
side effect of surgery for which levothyroxine replacement will be needed, lifelong.
Thyroidectomy
is a good treatment option for people with a large goitre and for those with thyroid eye
disease.
Prior to thyroid surgery, thyroid overactivity needs to be controlled, usually with
antithyroid drugs to
make an anaesthetic safe. This is because an anaesthetic in a hyperthyroid person has
a high risk
of precipitating a dangerous hyperthyroid crisis or thyrotoxic storm.
Treatment of thyroiditis
Many forms of thyroiditis are self-limiting, meaning that the overactivity recovers
spontaneously
and no treatment may be required. If the person has severe symptoms of
thyrotoxicosis,
betablockers are helpful. However, in some cases thyroiditis can be painful or
prolonged and antiinflammatory tablets or steroids may be helpful. Furthermore, in
some cases a period of thyroid
underactivity may follow the thyrotoxicosis, and this may require levothyroxine
treatment, if
causing severe symptoms.
Subclinical hyperthyroidism
In subclinical hyperthyroidism, the TSH is suppressed but the free thyroid hormone
levels are
normal. Endocrinologists regard this condition as a precursor of overt or clinical
hyperthyroidism
but there is some debate over whether this mildest of degree of hyperthyroidism
should be treated

(JAMA 2004; 291: 228-238, J Clin Endocrinol Metab. 2007 ;92:3-9.). Further
research is being
conducted in this area. At present treatment is a matter for individual clinical
evaluation and
discussion between patient and doctor, although there is a consensus that treatment
may be
worthwhile in the elderly, particularly if the heart rhythm becomes abnormal or there
is thinning of
the bones or low-impact bone fractures.
http://www.british-thyroid-association.org/info-forpatients/Docs/bta_patient_hyperthyroidism.pdf
13. Why the patient have that clinical manifestation ? explain
Palpitation: blood flow, cardiac output, cardiac deny frequency, and volume
of blood increases due to increased metabolism in tissue oxygen consumption
and increase speed up the final product is released from the tissue. This effect
causes vasodilation in most tissues of the body, thus increasing blood flow.
Fisiologi Guyton
Chronotropic and inotropic effects on the heart that is adding
increase the force of muscle contraction and heart rhythm.

Palpitation : Aliran darah, Curah jantung, Frekuensi deny jantung, dan Volume
darah meningkat karena meningkatnya metabolism dalam jaringan mempercepat
pemakaian oksigen dan memperbanyak produk akhir yang dilepas dari jaringan.
Efek ini menyebabkan vasodilatasi pada sebagian besar jaringan tubuh, sehingga
meningkatkan aliran darah. Guyton
Efek kronotropik dan Inotropik terhadap jantung yaitu menambah
kekuatan kontraksi otot dan menambah irama jantung.

It is difficult to sleep: Effects on sleep


o Because of the exhausting effects of thyroid hormone on muscle and
central nervous system, the hyperthyroid patients often feel tired
constantly, but because of the effects of thyroid hormone on the excitation
of the synapse, sleep difficulties arise. In contrast, a typical symptom of
severe somnolence hypothyroidism, accompanied by bedtime that lasts for
12-14 hours a day.

-FISIOLOGI KEDOKTERAN, Guyton

Sukar tidur: Efek pada tidur

Oleh karena efek yang melelahkan dari hormone tiroid pada otot dan
system saraf pusat, maka pasien hipertiroid sering merasa lelah terus
menerus, tetapi karena efek eksitasi dari hormone tiroid pada sinaps,
timbul kesulitan tidur. Sebaliknya, somnolen berat merupakan gejala
khas hipotiroidisme, disertai dengan waktu tidur yang berlangsung
selama 12-14 jam sehari.

-FISIOLOGI KEDOKTERAN, Guyton Why succumb hot?


Because BMR ride that ride thermogenesis. So the body can not
stand the heat.
Because of the patient's skin tends to soft thyrotoxicosis, warm,
and redness, patients often do not stand the heat.
Robbins n 'Kumar. PATHOLOGY. Vol 2. Edition 7. EGC
Mengapa tdk tahan panas ?
Karena BMR naik sehingga thermogenesis naik. Jadi tubuh tidak tahan panas.
Karena pada kulit pasien tirotoksikosis cenderung lunak, hangat, dan kemerahan,
pasien sering tidak tahan panas.
Robbins n Kumar. PATOLOGI. Vol 2. Edisi 7. EGC

Why do a lot of sweat?


Associated with central nervous system (causing the
dissociation of mind) anxiety and psychoneurotic, paranoia
always restless and sweating
Guyton Textbook of Physiology
Mengapa banyak keringat?

Berhubungan dengan sistem saraf pusat (menimbulkan disosiasi pikiran) cemas


dan psikoneurotik, paranoia selalu gelisah dan berkeringat
Buku Ajar Fisiologi Guyton

Why accomplish?
Because the debilitating effects of thyroid hormone on the
muscle and the central nervous system of patients with hyper
thyroid feel tired continuously.
Buku Ajar Fisiologi Guyton

Mengapa capai?
Karena efek yg melelahkan dari hormone tiroid
pada otot dan system syaraf pusat maka pasien
dengan hiper tiroid merasa lelah terus menerus.
Buku Ajar Fisiologi Guyton

Why is it weak?

Muscles in patients with hyperthyroidism will be weakened due


to protein catabolism superfluous.
Buku Ajar Fisiologi Guyton

Mengapa lemah?
Otot otot pada penderita hipertiroid akan menjadi
lemah dikarenakan adanya proses katabolisme
protein yg berlebihan.
Buku Ajar Fisiologi Guyton

Why shaking hands?


Increased thyroid hormone can also increase the strong muscle
contractions cause smooth muscle tremor, which is a typical
symptom of hyperthyroidism
Due to increased sensitivity of the nerve synapse in the medulla
that regulate muscle tone.
Buku Ajar Fisiologi Guyton

Mengapa tangan gemetar?


Peningkatan hormon tiroid juga dapat meningkatkan kontraksi
otot yang kuat menimbulkan tremor halus pada otot, yang
merupakan gejala khas hipertiroidisme

Disebabkan bertambahnya kepekaan sinaps syaraf di daerah medulla


yg mengatur tonus otot.
Buku Ajar Fisiologi Guyton

Why weight loss but increased appetite?


Increased sympathetic activity and hypermetabolism causes
weight loss despite increased appetite.
Robbins n 'Kumar. PATHOLOGY. Vol 2. Edition 7. EGC
Mengapa bb turun walau nafsu makan bertambah?
Peningkatan aktivitas simpatis dan hipermetabolisme menyebabkan penurunan BB
walaupun nafsu meningkat.
Robbins n Kumar. PATOLOGI. Vol 2. Edisi 7. EGC

Mengapa sering BAB?

Efek Gastrointestinal
Hormon tiroid merangsang motilitas usus, yang dapat menimbuklan
peningkatan motilitas dan diare pada hipertiroidisme dan memperlambat transit
usus serta konstipasi pada hipotiroidisme. Hal ini juga menyumbang pada
timbulnya penurunan berat badan yang sedang pada hipertiroidisme dan
pertambahan berat pada hipotiroidisme.
Pada saluran cerna, selain dapat meningkatkan nafsu
makan dan asupan makanan, hormone tiroid yang
meningatkat dapat mempercepat sekresi getah
pencernaan dan pergerakan saluran cerna, sehingga
sering terjadi diare

Mengapa sesak nafas bila kerja fisik?

14. Uncommon medical emergency caused by an exacerbation of hyperthyroidsim


characterized of one or more organ system in people with untreated and or poorly
treated hyperthyroidism. Hyperthyroid disease crisis usually occur in patient already
known to have hyperthyroidism but may be the first presentation of hyperthyroidism
early recognition and agressive treatment are essential.hyperthyroidism can occur in
patient w/ toxic adenoma or multinodular toxic goiter but its more often see in grave
disease. Hyperthyroidism crisis classically occurs in patient w/ underlying grave
disease or toxic multi nodular goiter often there is sudden onset of sever

hyperthyroidism with first hyperpyrexia over 41 celcius, dehidration, heart rate


greater 140/minutes, naussea, jundice, abdominal pain, confussion, seizeres(kejang),
comma
15. Krisis tiroid ?
A. definition
Thyroid crisis is a situation most severe clinical hyperthyroidism life-threatening, this
generally occurs in patients with Graves' disease foundation or toxic multinodular
goitre, and is associated with precipitating factors: infection, surgery, trauma,
substance iodized contrast, hypoglycemia, parturition, emotional stress, cessation of
anti-thyroid drugs, ketoacidosis, pulmonary thromboembolism, cerebrovascular
disease / stroke, thyroid palpas too strong.
A. Definisi
Krisis tiroid merupakan suatu keadaan klinis hipertiroidisme yang paling berat
mengancam jiwa, umumnya ini timbul pada pasien dengan dasar penyakit Graves atau
Struma multinodular toksik, dan berhubungan dengan faktor pencetus : infeksi, operasi,
trauma, zat kontras beriodium, hipoglikemia, partus, stress emosi, penghentian obat anti
tiroid, ketoasidosis, tromboemboli paru, penyakit serebrovaskuler/strok, palpas tiroid terlalu
kuat.
B. etiology
Thyroid crisis can occur due to dysfunction of the thyroid gland, the pituitary, or
hypothalamus, increased TSH thyroid gland malfunctions due to be accompanied by
decreased TSH and TRF as a negative feedback on the release of both HT.
Thyroid crisis due to malfunctions hipofisi gives an overview of HT and TSH levels are high.
TRF will be low because of negative feedback from HT and TSH. Thyroid crisis due to
malfunctioning hypothalamus will show a high HT accompanied by excessive TSH and TRH.
1. The main cause of
a. Grave's disease
b. Toxic multinodular
c. "Solitary toxic adenoma"
2. other causes
a. thyroiditis
b. troboblastis disease
c. Excessive intake of thyroid hormone
d. Excessive iodine consumption
e. pituitary cancer

f. Drugs such as amiodarone

B. Etiologi
Krisis tiroid dapat terjadi akibat disfungsi kelenjar tiroid, hipofisis, atau hipotalamus,
peningkatan TSH akibat malfungsi kelenjar tiroid akan disertai penurunan TSH dan TRF
karena umpan balik negatif HT terhadap pelepasan keduanya.
Krisis tiroid akibat malfungsi hipofisi memberikan gambaran kadar HT dan TSH yang
tinggi. TRF akan rendah karena umpan balik negatif dari HT dan TSH. Krisis tiroid akibat
malfungsi hipotalamus akan memperlihatkan HT yang tinggi disertai TSH dan TRH yang
berlebihan.
1

Penyebab utama
a

Penyakit Grave

Toxic multinodular

Solitary toxic adenoma

Penyebab lain
a

Tiroiditis

Penyakit troboblastis

Ambilan hormon tiroid secaraberlebihan

Pemakaianyodiumyangberlebihan

Kankerpituitari

ObatobatansepertiAmiodarone

Patofisiologi

G3 organik kelenjar tiroid

G3 Fungsi Hipotalamus /hipofisi

Produksi TSH meningkat

Produksi hormone
tiroid meningkat

Proses glikogenesis
meningkat

Metabolisme tubuh
meningkat

Produksi kalor
meningkat

Proses pembakaran lemak


meningkat

Aktifitas GI meningkat

Peningkatan suhu
tubuh

Suplai nutrisi yang tidak


adekuat

Nafsu makan meningkat

Penurunan berat badan

G3 rasa nyaman panas

G3 body image

Perubahan pola kerja


jantung dan paru

G3 pola kognitif

Ketidakstabilan emosi

Perubahan pola nutrisi

Clinical manifestations
1. Increased heart rate
2. Increased muscle tone, tremor, irritability, increased sensitivity to
catecholamines
3. Increase in basal metabolic rate, increased heat generation, heat
intolerance, excessive sweating
4. Weight loss, increased hunger (good appetite)
5. Increased frequency of bowel movements
6. Goiter (usually), which increased the size of the thyroid gland
7. reproductive disorders
8. Can not stand the heat
9. rapid fatigue
10. sign bruit
11. Menstruation bit and not fixed
12. Enlargement of the thyroid gland
13. Bulging eyes (exoptalmus)
Manifestasi klinis
1

Peningkatanfrekuensidenyutjantung

Peningkatan tonus otot, tremor, iritabilitas, peningkatan kepekaan terhadap


katekolamin

Peningkatan laju metabolisme basal, peningkatan pembentukan panas, intoleran


terhadappanas,keringatberlebihan

Penurunanberat,peningkatanrasalapar(nafsumakanbaik)

Peningkatanfrekuensibuangairbesar

Gondok(biasanya),yaitupeningkatanukurankelenjartiroid

Gangguanreproduksi

Tidaktahanpanas

Cepatletih

10 Tandabruit

11 Haidsedikitdantidaktetap
12 Pembesarankelenjartiroid
13 Matamelotot(exoptalmus)

Diagnosticexamination
Diagnosisdependsonseveralhormonesfollowing:
BloodteststhatmeasurelevelsofHT(T3andT4),TSH,andTRHwill
confirmthediagnosisandlocalizationproblemsatthestatelevelorcentral
nervoussystemthyroidgland.
1.TSH(ThyroidStimulatingHormone)
2.FreeT4(thyroxine)
3.FreeT3(triiodothyronine)
4.Diagnosismayalsobemadeusingultrabunyitoensuretheenlargementof
thethyroidgland
5.Thyroidscantoseeanenlargedthyroidgland
6.Hyperthyroidismcanbeaccompaniedbydecreasedserumlipidlevels
7.Decreaseinsensitivitytoinsulin,whichcancausehyperglycemia
PemeriksaanDiagnostik
Diagnosabergantungkepadabeberapahormonberikutini:
PemeriksaandarahyangmengukurkadarHT(T3danT4),TSH,danTRHakanmemastikan
diagnosis keadaan dan lokalisasi masalah di tingkat

susunan

sarafpusatataukelenjartiroid.
1

TSH(TiroidStimulating

Hormone)

BebasT4(tiroksin)

BebasT3(triiodotironin)

Diagnosajugabolehdibuatmenggunakanultrabunyiuntukmemastikanpembesaran
kelenjartiroid

Tiroidscanuntukmelihatpembesarankelenjartiroid

Hipertiroidismedapat
penurunankadarlemak

disertai
serum

Penurunankepekaanterhadapinsulin,yangdapat
menyebabkanhiperglikemia

Complication

Complicationsofthyroidcrisiscanbelifethreateningisthyrotoxic
crisis(thyroidstorm).Itcanberkernbangspontaneouslyhyperthyroid
patientswhounderwenttherapy,surgeryforthyroidgland,or
hyperthyroidismoccurinpatientswhoarenotdiagnosed.Theresultisthe
releaseofHTinverylargenumbersthatcausetachycardia,agitation,
tremors,hyperthermia(upto106F),and,ifuntreated,death.
HeartdiseaseHyperthyroidism,Gravesoftalmopati,dermopati
Graves,inthetreatmentofinfectionsduetoagranulocytosiswith
antithyroiddrugs.Thyroidcrisis:mortality
Komplikasi
Komplikasi Krisis tiroid yang dapat mengancam nyawa adalah krisis tirotoksik
(thyroid storm). Hal ini dapat berkernbang secara spontan pada pasien hipertiroid yang
menjalaniterapi,selamapembedahankelenjartiroid,atauterjadipadapasienhipertiroidyang
tidakterdiagnosis.AkibatnyaadalahpelepasanHTdalamjumlahyangsangatbesaryang
menyebabkan takikardia, agitasi, tremor, hipertermia (sampai 106F), dan, apabila tidak
diobati,kematian.
PenyakitjantungHipertiroid,oftalmopatiGraves,dermopatiGraves,infeksikarena
agranulositosispadapengobatandenganobatantitiroid.Krisistiroid:mortalitas

Management
1. conservative
Governance Graves disease
a. Anti-thyroid drugs. This drug inhibits the production of thyroid hormones. If
excessive doses, patients experience symptoms of drug hipotiroidisme.Contoh
are as follows:
1) Thioamide
2) Methimazole initial dose of 20 -30 mg / day

3) Propylthiouracil (PTU) initial dose of 300-600 mg / day, the maximum dose


of 2,000 mg / day
4) Potassium Iodide
5) Sodium Ipodate
6) Anion Inhibitors
b. Beta-adrenergic receptor antagonist. This medication is to reduce the
symptoms of hypothyroidism. Example: Propranolol
2. Surgical
a. Radioactive iodine.
This action is to destroy the thyroid gland is hyperactive
b. Thyroidectomy.
Surgery action is to remove the thyroid gland is enlarged
Penatalaksanaan
1

Konservatif
TatalaksanapenyakitGraves
a

Obat AntiTiroid. Obat ini menghambat produksi hormon tiroid. Jika dosis
berlebih, pasien mengalami gejala hipotiroidisme.Contoh obat adalah sebagai
berikut:
1

Thioamide

Methimazoledosisawal2030mg/hari

Propylthiouracil(PTU)dosisawal300600mg/hari,dosismaksimal2.000
mg/hari

PotassiumIodide

SodiumIpodate

AnionInhibitor

Betaadrenergic reseptor antagonist. Obat ini adalah untuk mengurangi gejala


gejalahipotiroidisme.Contoh:Propanolol

Surgical
a

Radioaktifiodine.

Tindakaniniadalahuntukmemusnahkankelenjartiroidyanghiperaktif
b

Tiroidektomi.
Tindakan Pembedahan

ini untuk

mengangkat kelenjar

tiroid

yangmembesar

Sumber:
1

Bare & Suzanne, 2002, Buku Ajar Keperawatan Medikal Bedah, Volume 2, (Edisi 8),
EGC, Jakarta.

Carpenito, 1999, Rencana Asuhan dan Dokumentasi Keperawatan, (Edisi 2), EGC,
Jakarta

Corwin,. J. Elizabeth, 2001, Patofisiologi, EGC, Jakarta

Doenges, E. Marilynn dan MF. Moorhouse, 2001, Rencana Asuhan Keperawatan, (Edisi
III), EGC, Jakarta.

FKUI, 1979, Patologi, FKUI, Jakarta


16. Explain the hypothyroid

Hypothyroidism is a disease caused by a disturbance in one of the levels of the hypothalamicpituitary-thyroid-"end organ", with the result of thyroid hormone deficiency, or impaired
tissue response to thyroid hormone.
According onset, hypothyroidism in children can be divided into two:
1. Congenital hypothyroidism.
2. Acquired hypothyroidism.
Hipotiroid adalah suatu penyakit yang disebabkan oleh gangguan pada salah satu tingkat dari
aksis hipotalamus-hipofisis-tiroid-end organ, dengan akibat terjadinya defisiensi hormon
tiroid, ataupun gangguan respon jaringan terhadap hormon tiroid.
Menurut onsetnya, hipotiroid pada anak dibedakan menjadi 2 :
1. Hipotiroid kongenital.
2. Hipotiroid dapatan.
Pathophysiology
Hypothyroidism can be caused by disruption of thyroid hormone synthesis or
disruption of tissue response to thyroid hormone.
Synthesis of thyroid hormones is regulated as follows:
- The hypothalamus makes "thyrotropin releasing hormone (TRH)" which stimulates
the anterior pituitary.
- Anterior pituitary synthesize thyrotropin ("TSH = thyroid stimulating hormone")
which stimulates the thyroid gland.
- The thyroid gland to synthesize thyroid hormone ("triiodothyronin = T3 = T4 =
tetraiodothyronin and thyroxin") which stimulates metabolism network includes: oxygen

consumption, body heat production, nerve function, metabolism protrein, carbohydrates,


fats, and vitamins, as well as work than other hormones.

PATOFISIOLOGI
Hipotiroid dapat disebabkan oleh gangguan sintesis hormon tiroid atau gangguan pada respon
jaringan terhadap hormon tiroid.
Sintesis hormon tiroid diatur sebagai berikut :
- Hipotalamus membuat thyrotropin releasing hormone (TRH) yang merangsang
hipofisis anterior.
- Hipofisis anterior mensintesis thyrotropin (thyroid stimulating hormone = TSH)
yang merangsang kelenjar tiroid.
- Kelenjar tiroid mensintesis hormone tiroid (triiodothyronin = T3 dan
tetraiodothyronin = T4 = thyroxin) yang merangsang metabolisme jaringan yang
meliputi : konsumsi oksigen, produksi panas tubuh, fungsi syaraf, metabolisme
protrein, karbohidrat, lemak, dan vitamin-vitamin, serta kerja daripada hormonhormon lain.
Clinical Symptoms
History and symptoms in neonates and infants:
- Fontanella major wide open posterior fontanel.
- Rectal temperature <35.5 C within 0-45 hours after birth.
- Birth weight> 3500 g; gestation> 40 weeks.
- Big and husky voice.
- Umbilical hernia.
- History of jaundice more than 3 days.
- Miksedema.
- Makroglosi.
- First Chapter History> 20 hours after birth and constipation (<1 time / day).
- Dry skin, cold, and "motling" (Stained-spotting).
- Lethargy.
- It is difficult to drink.
- Bradycardia (<100/minute).
Early diagnosis and treatment is important to prevent permanent mental patients.
Symptoms in older children:
- With or without goiter goiter.
- Impaired growth (dwarf).
- Impaired motor development, mental, teeth, bones, and puberty.
- Permanent disturbance of mental development, especially when onset occurs before
the age of 3 years.
- Reduced activity, slow.
- Dry skin.
- Miksedema.
- Low blood pressure, low metabolism.
- Intolerance to cold.
The causes of hypothyroidism:
- The causes of congenital (congenital):
o Disgenetik thyroid gland: ectopic, agenesis, or hipoplasi aplasi.
o Dishormonogenesis.
o 'the hypothalamic-pituitary hypothyroidism'.
o Be temporary:
Induction drugs.
maternal antibodies.
Idiopathic.
o Mother gets
Material goitrogen.
Treatment of radio-active iodine.
- The causes of acquired ("acquired"):

o
o
o
o
o
o
o

chronic lymphocytic thyroiditis.


goitrogen materials (iodine, tiourasil, etc.).
Thyroidectomy.
infiltrative disease (sistinosis, histiositosis-X).
iodine deficiency (endemic goiter).
"euthyroid sick syndrome".
hypopituitarism

GEJALA KLINIS
Riwayat dan gejala pada neonatus dan bayi :
- Fontanella mayor yang lebar dan fontanella posterior yang terbuka.
- Suhu rektal < 35,5C dalam 0-45 jam pasca lahir.
- Berat badan lahir > 3500 gram; masa kehamilan > 40 minggu.
- Suara besar dan parau.
- Hernia umbilikalis.
- Riwayat ikterus lebih dari 3 hari.
- Miksedema.
- Makroglosi.
- Riwayat BAB pertama > 20 jam setelah lahir dan sembelit (< 1 kali/hari).
- Kulit kering, dingin, dan motling (berbercak-bercak).
- Letargi.
- Sukar minum.
- Bradikardia (< 100/menit).
Diagnosis dan pengobatan dini penting untuk mencegah mental yang permanen pada
penderita.
Gejala pada anak besar :
- Dengan goiter maupun tanpa goiter.
- Gangguan pertumbuhan (kerdil).
- Gangguan perkembangan motorik, mental, gigi, tulang, dan pubertas.
- Ganguan perkembangan mental permanen terutama bila onset terjadi sebelum umur 3
tahun.
- Aktivitas berkurang, lambat.
- Kulit kering.
- Miksedema.
- Tekanan darah rendah, metabolisme rendah.
- Intoleransi terhadap dingin.
Sebab-sebab hipotiroid :
- Sebab-sebab bawaan (kongenital) :
o Disgenetik kelenjar tiroid: ektopik, agenesis, aplasi atau hipoplasi.
o Dishormonogenesis.
o Hypothalamic-pituitary hypothyroidism.
o Bersifat sementara :
Induksi obat-obatan.
Antibodi maternal.
Idiopatik.
o Ibu mendapat
Bahan goitrogen.
Pengobatan yodium radio-aktif.
- Sebab-sebab yang didapat (acquired):
o Tiroiditis limfositik menahun.
o Bahan-bahan goitrogen (yodium, tiourasil, dsb).

o
o
o
o
o

Tiroidektomi.
Penyakit infiltratif (sistinosis, histiositosis-X).
Defisiensi yodium (gondok endemik).
Euthyroid sick syndrome.
Hipopituitarisme

MANAGEMENT
Thyroid hormone
Drug of choice is L-Thyroxine Sodium, given as early as possible.
1. When the facility to measure thyroid function there, given the dose as the following
table:

Umur

Dosis g/kg BB/hari

0-3 bulan

10-15

3-6 bulan

8-10

6-12 bulan

6-8

1-5 tahun

5-6

2-12 tahun

4-5

> 12 tahun

2-3

T4 levels maintained in the mid-normal values.


2. When the facility to measure thyroid function does not exist, it can be done
therapeutic trial until the age of 3 years starting with a low dose in 2-3 weeks; when
there is clinical improvement, the dose can be increased gradually or at a dose of 100
+ g/m2/hari administration.
Thyroxine dose adjustment based on clinical response of thyroid function tests T3, T4,
and TSH which can vary depending on the etiology of hypothyroidism.

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PENATALAKSANAAN
Hormon tiroid
Obat pilihan adalah Sodium L-Thyroxine, diberikan sedini mungkin.
1. Bila fasilitas untuk mengukur faal tiroid ada, diberikan dosis seperti tabel berikut :
Umur

Dosis g/kg BB/hari

0-3 bulan

10-15

3-6 bulan

8-10

6-12 bulan

6-8

1-5 tahun

5-6

2-12 tahun

4-5

> 12 tahun

2-3

Kadar T4 dipertahankan di atas pertengahan nilai normal.

2.

Bila fasilitas untuk mengukur faal tiroid tidak ada, dapat dilakukan therapeutic
trial sampai usia 3 tahun dimulai dengan dosis rendah dalam 2-3 minggu; bila ada
perbaikan klinis, dosis dapat ditingkatkan bertahap atau dengan dosis
pemberian + 100 g/m2/hari.
Penyesuaian dosis tiroksin berdasarkan respon klinik dari uji fungsi tiroid T3, T4, dan
TSH yang dapat berbeda tergantung dari etiologi hipotiroid.
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DAFTAR PUSTAKA
1. Fisher DA. Disorders of the Thyroid in the Newborn and Infant. In : Sperling MA, ed.
Pediatric Endocrinology. Philadelphia : Saunders, 2002 : 161-82.
2. Styne DM. Disorders of the Thyroid Gland. In: Core Handbooks in Pediatrics Pediatric
Endocrinology. Philadelphia : Lippincott Williams & Wilkins, 2004 : 83-108.
3. Rossi WC, Caplin N, Alter CA. Thyroid Disorders in Children. In: Moshang T, ed.
Pediatric Endocrinology The Requisites in Pediatrics. St Louis, Missouri: Elsevier
Mosby, 2005 : 171-90.
4. Fort PF, Brown RS.Thyroid Disorders in Infancy. In : Lifshitz F,
ed. Pediatric Endocrinology. New York : Marcel Dekker, 1996 : 369-81.